Gut Microbiota of the Cabbage Looper, \u3ci\u3eTrichoplusia ni\u3c/i\u3e

The gut microbiome plays an essential role in the health of many organisms, including insects. Here we report initial findings of bacteria present in the caterpillar midgut of the cabbage looper, Trichoplusia ni, grown in lab conditions on artificial diet and identified using biochemical tests. We identified one species previously reported as part of the gut microbiota of Trichoplusia ni and three species not previously reported. Our results support the need for multiple types of bacterial identification when looking at gut microbiomes, with the most confidence in identification being when multiple tests are in agreement

IL-17 Signaling triggers degradation of the constitutive NF-κB inhibitor ABIN-1

IL-17 activates NF-κB and induces expression of proinflammatory genes. IL-17 drives disease in autoimmune conditions, and anti–IL-17 Abs have shown impressive success in the clinic. Although produced by lymphocytes, IL-17 predominantly signals in fibroblasts and epithelial cells. IL-17–driven inflammation is kept in check by negative feedback signaling molecules, including the ubiquitin editing enzyme A20, whose gene TNFAIP3 is linked to autoimmune disease susceptibility. The A20 binding inhibitor of NF-κB activation 1 (ABIN-1) is an A20-binding protein encoded by the TNIP1 gene, which is also linked to autoimmune disease susceptibility including psoriasis. Accordingly, we hypothesized that ABIN-1 might play a role in negatively regulating IL-17 signaling activity. Indeed, ABIN-1 enhanced both tonic and IL-17–dependent NF-κB signaling in IL-17–responsive fibroblast cells. Interestingly, the inhibitory activities of ABIN-1 on IL-17 signaling were independent of A20. ABIN-1 is a known NF-κB target gene, and we found that IL-17–induced activation of NF-κB led to enhanced ABIN-1 mRNA expression and promoter activity. Surprisingly, however, the ABIN-1 protein was inducibly degraded following IL-17 signaling in a proteasome-dependent manner. Thus, ABIN-1, acting independently of A20, restricts both baseline and IL-17–induced inflammatory gene expression. We conclude that IL-17–induced signals lead to degradation of ABIN-1, thereby releasing a constitutive cellular brake on NF-κB activation

IL-17 Receptor Signaling in Oral Epithelial Cells Is Critical for Protection against Oropharyngeal Candidiasis

Signaling through the IL-17 receptor (IL-17R) is required to prevent oropharyngeal candidiasis (OPC) in mice and humans. However, the IL-17-responsive cell type(s) that mediate protection are unknown. Using radiation chimeras we were able to rule out a requirement for IL-17RA in the hematopoietic compartment. We saw remarkable concordance of IL-17-controlled gene expression in C. albicans-infected human oral epithelial cells (OECs) and in tongue tissue from mice with OPC. To interrogate the role of the IL-17R in OECs, we generated mice with conditional deletion of IL-17RA in superficial oral and esophageal epithelial cells (Il17ra(ΔK13)). Following oral Candida infection, Il17ra(ΔK13) mice exhibited fungal loads and weight loss indistinguishable from Il17ra(−/−) mice. Susceptibility in Il17ra(ΔK13) mice correlated with expression of the antimicrobial peptide β-defensin 3 (BD3, Defb3). Consistently, Defb3(−/−) mice were susceptible to OPC. Thus, OECs dominantly control IL-17R-dependent responses to OPC through regulation of BD3expression

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

C/EBPβ^-/- mice exhibit increased susceptibility to oral candidiasis in the context of cortisone-induced immunosuppression.

<p><b>(A)</b> C65BL/6 mice (“WT”) were treated with the indicated doses of cortisone acetate at days -1, +1 and +2 relative to infection. After 5 d, fungal loads in tongue were assessed by CFU enumeration of tongue tissue homogenates. SHAM (n = 3), No cortisone control (n = 5), 60mg/kg (n = 9), 120/112mg/kg (n = 8), and 225mg/kg (n = 8). Data are pooled from 2 independent experiments. Bars indicate geometric mean with 95% CI. P<0.05 by t-test with Mann-Whitney correction: * vs NO CORT, ≠ vs 60mg/kg, # vs 120/112mg/kg and π vs 225mg/kg. (<b>B</b>) The indicated mice were infected orally as described in panel A. Cortisone acetate was administered subcutaneously on days -1, +1 and +2 relative to infection. C/EBPβ^+/+ SHAM (n = 3), C/EBPβ^+/+ (n = 5), C/EBPβ^+/+ 60 mg/kg (n = 16), C/EBPβ^+/- 60mg/kg (n = 16), C/EBPβ^-/- 60mg/kg (n = 10) and C/EBPβ^+/+ 225mg/kg (n = 4). <i>P</i><0.05 by t-test with Mann-Whitney correction: * vs C/EBPβ^+/+ NO CORT, ≠ vs C/EBPβ^+/+ 60mg/kg, # vs C/EBPβ^+/- 60mg/kg and π vs C/EBPβ^-/- 60mg/kg. Data are pooled from two independent experiments. <b>C.</b> Representative tongue sections from the indicated mice were stained with H&E or Periodic-acid Schiff (PAS). Scale bar indicates 200 μM. White arrows indicate hyphae.</p

Susceptibility of C/EBPβ^-/- mice to OPC correlates with expression of BD3.

<p><b>(A)</b> mRNA from tongue was isolated from the indicated mice 5 days after oral <i>C</i>. <i>albicans</i> infection [C/EBPβ^+/+ SHAM (n = 3), C/EBPβ^+/+ NO CORT (n = 3), C/EBPβ^+/+ 60mg/kg (n = 5), C/EBPβ^+/- 60mg/kg (n = 6), and C/EBPβ^-/- 60mg/kg (n = 5)]. Complementary DNA was prepared and subjected to qPCR analysis to detect the indicated genes. Results are presented as fold induction over SHAM treated mice and normalized to expression of <i>Gapdh</i>. Data are pooled from two independent experiments. <i>P</i><0.05 by student unpaired t-test. * vs C/EBPβ^+/+ NO CORT, ≠ vs C/EBPβ^+/+ 60mg/kg, # vs C/EBPβ^+/- 60mg/kg and π vs C/EBPβ^-/- 60mg/kg. (<b>B)</b> mRNA from tongue was isolated from the indicated mice 5 days after oral <i>C</i>. <i>albicans</i> infection and analyzed as in panel A. C/EBPβ^+/+ SHAM (n = 3), C/EBPβ^+/+ (n = 2), C/EBPβ^+/- (n = 2), and C/EBPβ^-/- (n = 2). Data are from one experiment. * <i>P</i><0.05 by student unpaired t-test. vs C/EBPβ^+/+, ≠ vs C/EBPβ^+/- and π vs C/EBPβ^-/-. (<b>C)</b> OKF6/TERT2 human oral keratinocytes were treated with 200 ng/ml IL-17 plus 2ng/ml TNFα or with 2×10⁶ HK <i>C</i>. <i>albicans</i> for 24 h. Complementary DNA was prepared and subjected to qPCR analysis to detect <i>DEFB4A</i>. Data are normalized to expression of <i>GAPDH</i> and represent absolute levels. Data are representative of 2 independent experiments. *<i>P</i><0.05 compared to unstimulated OKF6/TERT2 cells.</p

The susceptibility of C/EBPβ^-/- mice to OPC does not correlate with expression of prototypical IL-17-regulated genes.

<p>mRNA from tongue was isolated from the indicated mice 5 days after oral <i>C</i>. <i>albicans</i> infection [C/EBPβ^+/+ SHAM (n = 3), C/EBPβ^+/+ NO CORT (n = 3), C/EBPβ^+/+ 60mg/kg (n = 5), C/EBPβ^+/- 60mg/kg (n = 6), and C/EBPβ^-/- 60mg/kg (n = 5)]. Complementary DNA was prepared and subjected to qPCR analysis to detect the indicated genes. Results are presented as fold induction over SHAM treated mice and normalized to expression of <i>Gapdh</i>. Data are pooled from 2 independent experiments. <i>P</i><0.05 by student unpaired t-test: * vs C/EBPβ^+/+ NO CORT, ≠ vs C/EBPβ^+/+ 60mg/kg, # vs C/EBPβ^+/- 60mg/kg and π vs C/EBPβ^-/- 60mg/kg.</p

(Simpson-Abelson <i>et al</i>.).

<p>Transcript expression levels of the indicated genes in tongues isolated from the indicated mice 5 days after induction of oropharyngeal candidiasis. Increase over Sham-infected mice is indicated as follows:</p><p>*2-4-fold,</p><p>** 5–10 fold,</p><p>*** 10–50 fold,</p><p>**** > 100-fold</p><p>(Simpson-Abelson <i>et al</i>.).</p

C/EBPβ^-/- mice exhibit increased susceptibility to systemic candidiasis but are resistant to oral candidiasis.

<p>(<b>A</b>) The indicated mice (n = 3 per group) were injected with <i>C</i>. <i>albicans</i> in the lateral tail vein. Time to sacrifice is indicated (days). *<i>P</i><0.05 versus (vs) C/EBPβ^+/- mice using Log-rank (Mantel-Cox). (<b>B</b>) The indicated mice were infected sublingually with <i>C</i>. <i>albicans</i> for 75 mins. After 5 d, fungal loads in tongue were assessed by CFU enumeration of tongue tissue homogenates. Bars indicate geometric mean with 95% CI. C/EBPβ^+/+ SHAM (n = 3), C/EBPβ^+/+ (n = 5), C/EBPβ^+/- (n = 9), C/EBPβ^-/- (n = 3), C/EBPβ^+/+ plus 225mg/kg cortisone (n = 3); cortisone acetate was administered by subcutaneous injection on days -1, +1 and +2 relative to infection. <i>P</i><0.05 by t-test with Mann-Whitney correction: * vs C/EBPβ^+/+ WT, ≠ vs C/EBPβ^+/-, # vs C/EBPβ^-/-, π vs C/EBPβ^+/+ 225mg/kg. <b>C</b>. Weights of mice were assessed daily and graphed as percent of starting weight. * vs C/EBPβ^+/+ WT. <i>P</i><0.05 by t-test with Mann-Whitney correction. Experiment was performed once.</p

How will mosquitoes adapt to climate warming?

The potential for adaptive evolution to enable species persistence under a changing climate is one of the most important questions for understanding impacts of future climate change. Climate adaptation may be particularly likely for short-lived ectotherms, including many pest, pathogen, and vector species. For these taxa, estimating climate adaptive potential is critical for accurate predictive modeling and public health preparedness. Here, we demonstrate how a simple theoretical framework used in conservation biology—evolutionary rescue models—can be used to investigate the potential for climate adaptation in these taxa, using mosquito thermal adaptation as a focal case. Synthesizing current evidence, we find that short mosquito generation times, high population growth rates, and strong temperature-imposed selection favor thermal adaptation. However, knowledge gaps about the extent of phenotypic and genotypic variation in thermal tolerance within mosquito populations, the environmental sensitivity of selection, and the role of phenotypic plasticity constrain our ability to make more precise estimates. We describe how common garden and selection experiments can be used to fill these data gaps. Lastly, we investigate the consequences of mosquito climate adaptation on disease transmission using Aedes aegypti-transmitted dengue virus in Northern Brazil as a case study. The approach outlined here can be applied to any disease vector or pest species and type of environmental change